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Retracted : Overexpression of long noncoding RNA SLC26A4‐AS1 inhibits the epithelial–mesenchymal transition via the MAPK pathway in papillary thyroid carcinoma
Author(s) -
Wang DuoPing,
Tang XiaoZhun,
Liang QuanKun,
Zeng XianJie,
Yang JianBo,
Xu Jian
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29145
Subject(s) - mapk/erk pathway , cancer research , epithelial–mesenchymal transition , vimentin , long non coding rna , thyroid carcinoma , biology , antisense rna , transfection , apoptosis , cell growth , kinase , downregulation and upregulation , rna , cell culture , gene , microbiology and biotechnology , thyroid , immunohistochemistry , endocrinology , immunology , genetics
Papillary thyroid carcinoma (PTC) is recognized as one of the most prevalent types of thyroid cancer with poor prognosis. Long noncoding RNA (lncRNA) has undergone an intensive study for their involvement in tumor treatment. This study intends to unravel the association of lncRNA SLC26A4‐AS1 with PTC. Initially, PTC‐related expression profiling data (GSE33630) was utilized to screen differentially expressed lncRNAs in PTC and the underlying mechanisms involved with the mitogen‐activated protein kinase (MAPK) pathway. Moreover, PTC tumor tissues and paracancerous tissues were arranged to determine expressions of TP53, SLC26A4‐AS1, and genes related to epithelial–mesenchymal transition (EMT) and the MAPK pathway. Furthermore, SLC26A4‐AS1 was overexpressed or underexpressed and JNK was underexpressed through cell transfection to examine the effect of SLC26A4‐AS1 on PTC via MAPK pathway. Besides, tumor formation in nude mice was used to verify the fore experiment. LncRNA SLC26A4‐AS1 regulating TP53 had the potential to participate in PTC by regulating the MAPK pathway. SLC26A4‐AS1 was expressed poorly in PTC. Notably, SLC26A4‐AS1 elevated E‐cadherin expression while it reduced that of ERK and Vimentin. In addition, the overexpression of SLC26A4‐AS1 inactivated the MAPK pathway by promoting TP53 and decreased cell migration, proliferation, and invasion. In addition to all these effects, the overexpression of SLC26A4‐AS1 promoted apoptosis of TPC‐1 cells. Additionally, the overexpression of lncRNA SLC26A4‐AS1 reduced xenograft tumor volume in nude mice. Furthermore, the effect of SLC26A4‐AS1 overexpression was found to be promoted after the MAPK pathway inactivation. Taken together, the overexpression of lncRNA SLC26A4‐AS1 coffered anti‐oncogenic effects on PTC through the inactivation of the MAPK pathway.